YTHDF3 Modulates EGFR/ATK/ERK/p21 Signaling Axis to Promote Cancer Progression and Osimertinib Resistance of Glioblastoma Cells.
EGFR
GBM
Osimertinib
Osimertinib resistance
YTHDF3
p21
senescence
stemness
Journal
Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988
Informations de publication
Date de publication:
Dec 2023
Dec 2023
Historique:
received:
24
09
2023
revised:
03
11
2023
accepted:
07
11
2023
medline:
1
12
2023
pubmed:
30
11
2023
entrez:
29
11
2023
Statut:
ppublish
Résumé
Despite recent advances in EGFR-tyrosine kinase inhibitor (TKI) drugs for glioblastoma multiforme (GBM), intrinsic EGFR alterations in GBM have resulted in drug resistance and unsatisfactory clinical development of EGFR-TKIs. Determining the unknown mechanisms underlying EGFR-TKI drug resistance is an urgent, but unmet, medical need for GBM. Although several m Osimertinib-resistant GBM cells (U87 YTHDF3 played a crucial role in inducing cellular proliferation, migration, and stemness in U87 Overall, our research underscores the novel potential of YTHDF3 as a new pharmacological target in GBM treatment, specifically for patients with osimertinib-resistant or refractory tumors.
Sections du résumé
BACKGROUND/AIM
OBJECTIVE
Despite recent advances in EGFR-tyrosine kinase inhibitor (TKI) drugs for glioblastoma multiforme (GBM), intrinsic EGFR alterations in GBM have resulted in drug resistance and unsatisfactory clinical development of EGFR-TKIs. Determining the unknown mechanisms underlying EGFR-TKI drug resistance is an urgent, but unmet, medical need for GBM. Although several m
MATERIALS AND METHODS
METHODS
Osimertinib-resistant GBM cells (U87
RESULTS
RESULTS
YTHDF3 played a crucial role in inducing cellular proliferation, migration, and stemness in U87
CONCLUSION
CONCLUSIONS
Overall, our research underscores the novel potential of YTHDF3 as a new pharmacological target in GBM treatment, specifically for patients with osimertinib-resistant or refractory tumors.
Identifiants
pubmed: 38030188
pii: 43/12/5485
doi: 10.21873/anticanres.16751
doi:
Substances chimiques
Aniline Compounds
0
EGFR protein, human
EC 2.7.10.1
ErbB Receptors
EC 2.7.10.1
osimertinib
3C06JJ0Z2O
Protein Kinase Inhibitors
0
YTHDF3 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
5485-5498Informations de copyright
Copyright © 2023 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.